We found that both SPI-1 (ΔinvA) and SPI-2 (ΔssaR) mutations on an ΔaroA background caused significantly lower bacterial colonization (Figure 1A) as well as significantly lower numbers of neutrophils in the cecum of infected mice (Figure 1B), similar to what has been previously reported with infections with the wild-type strain. The gene discussed is SPI1; the disease is infection.